Cirugía fetal experimental en un modelo animal para la corrección de mielomeningocele / Experimental fetal surgery in an animal model for the correction of myelomeningocele

Introducción. El mielomeningocele representa una de las malformaciones congénitas más frecuentes y severas en humanos, que afecta aproximadamente a 1 de cada 2.000 recién nacidos en el mundo. Tiene una enorme significación médica y social, por la importante morbilidad a que se asocia, con gran cantidad de secuelas y un elevado coste en salud. Existe sólida evidencia que apoya la necesidad de tratamiento precoz. Dentro de las posibilidades de tratamiento actuales tiene especial interés la reparación quirúrgica durante la vida intrauterina. El trabajo con un modelo animal constituye el paso previo necesario a la intervención en humanos. Objetivos. En concordancia con otros grupos de investigadores, hemos elegido un modelo animal que permita conocer los resultados de la reparación de la columna vertebral en mielomenigoceles creados instrumentalmente. Material y métodos. Durante el período de mayo de 2002 hasta mayo de 2004 se ha reclutado un grupo de 23 ovejas de raza merina a las que se les realizó quirúrgicamente, a los 80 días de preñez, un mielomeningocele, realizando una laminectomía lumbar de 1 a 4 con apertura del canal medular y exposición del contenido al líquido amniótico. Las ovejas fueron aleatorizadas para ser incluidas en tres grupos: un grupo control y dos grupos de intervención. En uno de ellos se realizó una reparación neuroquirúrgica convencional y en el otro grupo se realizó una reparación colocando una membrana de tejido dérmico porcino acelular cultivado. Resultados. Los corderos del grupo control nacieron con manifestaciones clínicas severas de la enfermedad (tres de cinco corderos), con incapacidad en la deambulación e incontinencia de esfínteres; en los corderos de ambos grupos de intervención las manifestaciones clínicas de espina bífida fueron leves (cuatro de cinco corderos), con dificultad leve en la deambulación y continencia de esfínteres. Conclusiones. Los resultados alcanzados por el trabajo, debido al reducido número de intervenciones, no son concluyentes, pero muestran una tendencia a favor de la intervención de reparación intraútero del mielomeningocele. Las consecuencias de estos resultados en la práctica clínica deberán ser observadas a la luz de los resultados del Management of Myelomeningocele Study (MOMS) que se desarrolla actualmente en Estados Unidos en cuatro centros. Comentario final. La realización del presente trabajo ha tenido enorme significación para los autores ya que se ha reunido un equipo multidisciplinario que incluye anestesiólogos, neurocirujanos, neonatólogos, obstetras, veterinarios, enfermeros, neurólogos, etc., y se ha alcanzado el objetivo de adquirir nuevas destrezas que serán fundamentales para el manejo futuro de la cirugía fetal intraútero (AU)

Introduction. Myelomeningocele is one of the most frequent and severe congenital defects in humans, affecting approximately one in 2000 worldwide. This pathology is of great medical and social relevance due to its high morbidity, multiple sequela and high social cost. There is supporting evidence in favor of early treatment, particularly through intra uterine surgical correction. The work on animal models is a required preliminary step before intervention on humans. Objectives. In agreement with several other investigative groups we have chosen an animal model that allows us to know the results of spine correction in surgically induced myelomeningocele. Material and methods. Between may of 2002 and may of 2004 we recruited 23 sheep on which we induced myelomeningocele surgically at 80 days of gestational age, through 1 to 4 lumbar laminectomy with opening of bone marrow channel and exposure to amniotic fluid. AH sheep were randomized to be included in three groups: control group A, and intervention groups B (conventional intervention) and C (conventional plus noncellular porcine skin patch. Results. Neonate lambs (three out of five) in the control group presented with severe clinical disease related disabilities, namely walking impairment and incontinence. Lambs in B and C groups showed less severe impairment: slight walking handicap and lack of incontinence. Conclusions. Owing to the small sampling the results we reached are not conclusive, though they show a trend in favor of intrauterine correction of myelomeningocele. Relevance of these findings should be availed for clinical practice through the results from Management of Myelomeningocele Study (MOMS), currently ongoing in four UScenters. Final comment. The present trial represents an important advance for all participants in that it gathered a multidisciplinary team composed of anesthesiologists, neurosurgeons, pediatric neurosurgeons, obstetricians, pediatricians, vets, nurses, etc., and has led us to the acquisition of essential handskills for the future management of intra uterine fetal surgery (AU)

Microespuma exoperimental aplicada en venas de animales de laboratorio / Experimental Microfoam applied to veins of laboratory animals

La vedette actual de la escleroterapia es la Microespuma. Logramos inocular una "mousse" de esclerosante en dos especies animales-conejos y ovinos-obteniendo resultados sorprendentes. La fórmula detallada de la microespuma es no tóxica, de muy fácil manejo y por sobre todo económica. Se utilizaron estas dos especies animales por las siguientes razones:-La estructura histológica del endotelio vascular del conejo es la más semejante al humano.-Los conejos fueron inoculados para evaluar venas de pequeño calibre,0.4-1.5mm, mientras que los ovinos para evaluar venas de calibre medianoi, 1.5-3.0 mm aproximadamente

Microespuma exoperimental aplicada en venas de animales de laboratorio / Experimental Microfoam applied to veins of laboratory animals

La vedette actual de la escleroterapia es la Microespuma. Logramos inocular una "mousse" de esclerosante en dos especies animales-conejos y ovinos-obteniendo resultados sorprendentes. La fórmula detallada de la microespuma es no tóxica, de muy fácil manejo y por sobre todo económica. Se utilizaron estas dos especies animales por las siguientes razones:-La estructura histológica del endotelio vascular del conejo es la más semejante al humano.-Los conejos fueron inoculados para evaluar venas de pequeño calibre,0.4-1.5mm, mientras que los ovinos para evaluar venas de calibre medianoi, 1.5-3.0 mm aproximadamente

Modelo experimental de infeccion por Helicobacter pylori en el raton. Estudio del dano gastrico producido por indometacina / Experimental model of infection of Helicobacter pylori in the mouse. A study of gastric damage caused by indomethacin

INTRODUCTION: The action of non-steroidal anti-inflammatory drugs (NSAIDs) on the Helicobacter Pylori (Hp) infected mucosa is a matter of debate. Some authors consider them to cause additive iatrogeny whilst others attribute a purportedly protective action to them. The development of on experimental animal model could help clarify this phenomenon. OBJECTIVES: 1--To develop an animal model of Hp gastric infection. 2--To evaluate the aggressiveness of NSAIDs in this model. MATERIALS AND METHODS: Male 6 month old BALC/C mice weighing 38 g were studied. Pylori Hp infection was ruled out. On three occasions, in the same week, 18 mice were inoculated intra-gastrically with 0.6 ml of Hp culture broth (brain-heart infusion) containing 1 x 10 8-1 x 10 9 CFU/ml. Another group of mice were inoculated with sterile saline. After two months the mice were killed and their stomachs studied. They were divided into groups: a) 6 Hp negative control mice. b) 8 Hp negative mice with prior intra-peritoneal injection of 25 mg/Kg indomethacin (24 hs.) c) 8 mice inoculated with Hp with indomethacin. d) 8 mice inoculated with Hp, without indomethacin. The stomachs were opened along the greater curvature and photographed macroscopically in order to map the necrotic area. The antrums were biopsied to test for urease and separate antrum and body specimens were send for staining with Warthin-Starry H & B and histopathology. RESULTS: All the mice inoculated with Hp acquired the infection. The necrotic area was larger in Group B: 55.5 +/- 7.87 mm than in Group C: 15 +/- 1.82 mm P < 0.00019. HISTOLOGY: Group A: normal mucosa. Group B: extensive coagulation necrosis and focal erosions. Group C: ulcers with inflammatory infiltrate and smaller necrotic area, presence of Hp on the surface epithelium. Group D: no ulcers, Hp present. CONCLUSION: An animal model of Hp infection was successfully developed Hp infection could play a potentially protective role against indomethacin aggression in the mouse.

Modelo experimental de infección por Helicobacter pylori en el ratón. Estudio del daño gástrico producido por indometacina. / [Experimental model of infection of Helicobacter pylori in the mouse. A study of gastric damage caused by indomethacin]

INTRODUCTION: The action of non-steroidal anti-inflammatory drugs (NSAIDs) on the Helicobacter Pylori (Hp) infected mucosa is a matter of debate. Some authors consider them to cause additive iatrogeny whilst others attribute a purportedly protective action to them. The development of on experimental animal model could help clarify this phenomenon. OBJECTIVES: 1--To develop an animal model of Hp gastric infection. 2--To evaluate the aggressiveness of NSAIDs in this model. MATERIALS AND METHODS: Male 6 month old BALC/C mice weighing 38 g were studied. Pylori Hp infection was ruled out. On three occasions, in the same week, 18 mice were inoculated intra-gastrically with 0.6 ml of Hp culture broth (brain-heart infusion) containing 1 x 10 8-1 x 10 9 CFU/ml. Another group of mice were inoculated with sterile saline. After two months the mice were killed and their stomachs studied. They were divided into groups: a) 6 Hp negative control mice. b) 8 Hp negative mice with prior intra-peritoneal injection of 25 mg/Kg indomethacin (24 hs.) c) 8 mice inoculated with Hp with indomethacin. d) 8 mice inoculated with Hp, without indomethacin. The stomachs were opened along the greater curvature and photographed macroscopically in order to map the necrotic area. The antrums were biopsied to test for urease and separate antrum and body specimens were send for staining with Warthin-Starry H & B and histopathology. RESULTS: All the mice inoculated with Hp acquired the infection. The necrotic area was larger in Group B: 55.5 +/- 7.87 mm than in Group C: 15 +/- 1.82 mm P < 0.00019. HISTOLOGY: Group A: normal mucosa. Group B: extensive coagulation necrosis and focal erosions. Group C: ulcers with inflammatory infiltrate and smaller necrotic area, presence of Hp on the surface epithelium. Group D: no ulcers, Hp present. CONCLUSION: An animal model of Hp infection was successfully developed Hp infection could play a potentially protective role against indomethacin aggression in the mouse.

Modelo experimental de infeccion por Helicobacter pylori en el raton. Estudio del dano gastrico producido por indometacina / Experimental model of infection of Helicobacter pylori in the mouse. A study of gastric damage caused by indomethacin

INTRODUCTION: The action of non-steroidal anti-inflammatory drugs (NSAIDs) on the Helicobacter Pylori (Hp) infected mucosa is a matter of debate. Some authors consider them to cause additive iatrogeny whilst others attribute a purportedly protective action to them. The development of on experimental animal model could help clarify this phenomenon. OBJECTIVES: 1--To develop an animal model of Hp gastric infection. 2--To evaluate the aggressiveness of NSAIDs in this model. MATERIALS AND METHODS: Male 6 month old BALC/C mice weighing 38 g were studied. Pylori Hp infection was ruled out. On three occasions, in the same week, 18 mice were inoculated intra-gastrically with 0.6 ml of Hp culture broth (brain-heart infusion) containing 1 x 10 8-1 x 10 9 CFU/ml. Another group of mice were inoculated with sterile saline. After two months the mice were killed and their stomachs studied. They were divided into groups: a) 6 Hp negative control mice. b) 8 Hp negative mice with prior intra-peritoneal injection of 25 mg/Kg indomethacin (24 hs.) c) 8 mice inoculated with Hp with indomethacin. d) 8 mice inoculated with Hp, without indomethacin. The stomachs were opened along the greater curvature and photographed macroscopically in order to map the necrotic area. The antrums were biopsied to test for urease and separate antrum and body specimens were send for staining with Warthin-Starry H & B and histopathology. RESULTS: All the mice inoculated with Hp acquired the infection. The necrotic area was larger in Group B: 55.5 +/- 7.87 mm than in Group C: 15 +/- 1.82 mm P < 0.00019. HISTOLOGY: Group A: normal mucosa. Group B: extensive coagulation necrosis and focal erosions. Group C: ulcers with inflammatory infiltrate and smaller necrotic area, presence of Hp on the surface epithelium. Group D: no ulcers, Hp present. CONCLUSION: An animal model of Hp infection was successfully developed Hp infection could play a potentially protective role against indomethacin aggression in the mouse. (AU)